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Cancer copies how healthy cells move to invade organs

By Michael Slezak

To slip, slide, squeeze and otherwise invade different parts of the body, cancer cells learn to switch between two modes of moving usually used by healthy cells. Now we know how.

For a cancer cell, the body is like a complex obstacle course, says Erik Sahai from Cancer Research UK in London. “If it is to spread from one part of the body to another, it will encounter a diverse range of tissue environments.”

To complete the obstacle course, the cancer cells need to move in different ways depending on the tissue they are confronted with. They learn how by mimicking the ways other types of cell move around the body. For example, when you scratch your skin, fibroblasts move in to help the wound heal, using adhesive forces to slide forward. If the scratch gets infected, white blood cells rush in, propelling themselves using electrostatic forces, among others.

Many invasive cancers have learned both methods, switching between them to suit their environment. “Being able to switch is likely to be the most important factor in making a cancer cell dangerous,” says Sahai.

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Movement mutation

To find out how they do this, Sahai and his colleagues looked at cells moving in the egg sac of fruit flies and tweaked the fly genes, altering the proteins they create. This allowed them to work out which proteins are important for movement. Next, they searched databases to see if any of those they identified also go awry in cancer, hitting upon a bundle called the STRIPAK complex. In many cancers, the gene that codes for these proteins is mutated.

“The STRIPAK complex enables cancer cells to move in both ways, without it they are locked into the more ‘fibroblastic’ mode and are therefore less dangerous,” says Sahai.

Sahai and colleagues have uncovered what could be a “cornerstone” of cancer’s invasive behaviour, says Maté Biro from the University of Sydney in Australia. “Whilst still far removed from a direct application at the bedside, this study opens new doors for therapeutic developments that could be applicable to a broad range of solid cancers,” he says.

Sahai says the obvious thing to look at next is whether people with this mutation are more likely to have an invasive cancer, which could help guide treatment. Further afield, researchers could even try to block the production of some of the STRIPAK proteins. Although Biro notes that this could be counterproductive since they may be central to the way immune cells or other cells move around the body.